Hui Chen

Cerebrospinal fluid (CSF) surrounding the optic nerve is essential for nutrient transport, waste removal, and optic nerve function. Optic disc edema in astronauts during long-duration spaceflight-Spaceflight Associated Neuro-Ocular Syndrome (SANS)-may result from impaired optic nerve CSF drainage, but the drainage pathway remains unclear. Given that the optic nerve sheath is an extension of the cranial meninges, we hypothesized that its CSF drains via lymphatic vessels rather than refluxing into the cranium. We assessed the pressure relationship between intracranial and optic nerve CSF and traced its drainage pathway. Our results show that optic nerve sheath CSF pressure is consistently lower than intracranial pressure, with no reflux observed. Instead, optic nerve CSF drains into deep cervical lymph nodes via lymphatic vessels within the sheath. These findings provide new insights into optic nerve CSF dynamics and may help elucidate SANS pathogenesis.

The cerebrospinal fluid (CSF) surrounding the optic nerve (to differentiate with the intracranial CSF, it is named as optic nerve CSF) plays important roles in nutrient exchange, waste removal, and maintenance of optic nerve function. Recent studies have suggested that the optic disc edema observed in astronauts may be linked to the retention of CSF around the optic nerve, and this retention may even be derived from impaired drainage of optic nerve CSF. However, how the optic nerve CSF is drained out remains inconclusive. We speculated that the optic nerve CSF may be drained out through lymphatic vessels of the optic nerve sheath. Here, we found by immunofluorescence and in vivo fluorescence imaging that, in both rats and humans, the optic nerve sheath has lymphatic vessels. Furthermore, we observed that the pressure in the optic nerve CSF is lower than the intracranial pressure, and the optic nerve CSF does not reflux into the intracranial space but is, instead, drained out into the deep cervical lymph nodes (dcLNs) through the lymphatic vessels in the optic nerve sheath. These observations have significant implications for understanding the physiological turnover and drainage pathways of optic nerve CSF. It may also help better understand the pathogenesis underlying spaceflight and Spaceflight Associated Neuro-Ocular Syndrome (SANS).

Ten novel MHC‐DPA1 alleles were identified in Tibetan macaques ( Macaca thibetana ).

Thyroid-associated ophthalmopathy (TAO) is an autoimmune orbital disease influenced by multiple factors, including genetic and immune factors. The enlargement of orbital fat tissues are mainly due to abnormal activation of adipocyte differentiation. Epigenetic modifications provide mechanistic insight for regulating gene expression and cellular differentiation. Lysine specific demethylase 1 (LSD1) is reported in regulation of adipogenesis. Therefore, it is critical to investigate the relationship between epigenetic modifier LSD1 and histone modification level during TAO process. In this study, combined with the clinic study and highthrough sequencing approach, our results revealed that the volume of orbital fat tissue was lower in TAO patients compared to non-TAO patients, whereas the number of adipocytes was higher in TAO patients compared to non-TAO patients, the expression level of adipocyte differentiation markers were higher in TAO samples. Consistently, at the cellular system, the expression level of adipogenic markers were higher in the TAO derived cells compared with the non-TAO cells. And we found LSD1 was highly expressed in TAO-derived cells. However, knocking down LSD1 decreased the expression of adipocyte markers. Mechanistically, LSD1 promoted adipocyte gene activation by demethylating H3K9me2 at the promoter regions. Finally, treatment with pargyline, an LSD1 inhibitor, inhibited adipogenesis in a dose-dependent manner, and the same inhibition of adipogenesis results were obtained with treatment with teprotumumab alone or combined with pargyline. Overall, our study indicates that epigenetic modifications were dysregulated in TAO process, and these data elucidated a novel mechanism of adipocyte differentiation during TAO progression and positioned LSD1 as a potential anti-adipogenesis target in TAO. Further understanding of the interaction betwen transcription factors and epigeneic modifiers or other histone modifications in TAO is essential for providing new perspectives in TAO mechanistic study and clinical intervention.

Recent research advancements have enhanced our understanding of the lymphatic system in the eye and nasal region and its involvement in health and disease. The eye is an anatomical extension of the central nervous system and was previously believed to be devoid of lymphatic structures, except for the conjunctiva. However, Lymphatic vessels have been recently identified in the cornea (under pathological conditions), limbus, ciliary body, extraocular muscles, conjunctiva, lacrimal gland, optic nerve sheath, and lymphoid structures in the choroid and Schlemm’s duct. These novel findings have significant implications in eye disease treatment; however, the mechanisms by which they preserve immune balance in the eye and eliminate metabolic waste and inflammatory cells remain nebulous. Furthermore, connections have been observed between ocular and nasal lymphatic vessels via the lymphatic network accompanying the nasolacrimal duct. The nasal lymphatic vessels are the primary pathway for cerebrospinal fluid drainage and a new route for drug delivery and treatment of brain-related diseases. This review provides an overview of recent advancements in understanding the structure and function of the ocular and nasal lymphatic systems and their association with cerebrospinal fluid drainage and various diseases.

Spaceflight-associated neuro-ocular syndrome (SANS) has been well documented in astronauts. However, its pathogenesis is not fully understood. New findings indicate the impaired outflow of the optic nerve cerebrospinal fluid may participate or contribute to some changes in SANS. In this perspective, we generated a hypothesis that the outflow of cerebrospinal fluid through the optic nerve sheath may be impaired under micro-gravity and then may potentially lead to SANS-related alterations.

In recent years, an increasing number of scientists have focused on conducting experiments on laser ablation of bone tissue. The purpose of this study was to summarize the prognosis of tissue and the extent of thermal damage in past hard tissue ablation experiments, and review the evidence for the feasibility of laser osteotomy in surgery. An electronic search of PubMed, China National Knowledge Infrastructure (CNKI), and Web of Science (WOS) for relevant English-language articles published through June 2023 was conducted. This review includes 48 literature reports on laser ablation of hard tissues from medical and biological perspectives. It summarizes previous studies in which the ideal ablation rate, depth of ablation, and minimal damage to bone tissue and surrounding soft tissues were achieved by changing the laser type, optimizing the laser parameter settings, or adding adjuvant devices. By observing their post-operative healing and inflammatory response, this review aims to provide a better understanding of pulsed laser ablation of hard tissues. Previous studies suggest that laser osteotomy has yielded encouraging results in bone resection procedures. We believe that low or even no thermal damage can be achieved by experimentally selecting a suitable laser type, optimizing laser parameters such as pulse duration and frequency, or adding additional auxiliary cooling devices. However, the lack of clinical studies makes it difficult to conclusively determine whether laser osteotomy is superior in clinical applications.

Introduction Progressive cerebral venous sinus thrombosis (CVST)-induced visual loss remains problematic, despite decreasing overall mortality owing to early diagnosis and aggressive treatment. Optic nerve sheath fenestration (ONSF) improves or stabilizes visual function in patients with idiopathic intracranial hypertension; however, its role in CVST awaits elucidation. We evaluated the efficacy and safety of ONSF in resolving CVST-induced visual impairment based on long-term observation. Methods This observational study included 18 patients with progressive CVST-induced visual loss, who had undergone ONSF between 2012 and 2021. Patients received maximum medical therapy, including anticoagulants and intracranial pressure (ICP)-lowering medications. The best-corrected visual acuity (BCVA), visual fields (VFs), and optic nerve head were assessed at baseline, at 1 week after ONSF, and over 6 months after ONSF. Activities of daily living (ADL) and National Eye Institute Visual Function Questionnaire-25 (VFQ-25) scores were assessed at final follow-up. Results Thirty-one ONSF-treated eyes of 18 patients were included. The mean follow-up duration was 35.6 months (range 1 week–8 years). Two patients were lost to follow-up. Before ONSF, all patients were still experiencing progressive visual loss despite receiving adequate anticoagulation and ICP-lowering therapy. Postoperative BCVA remained stable or improved in 25/31 eyes (80.6%) 1 week postoperatively and 17/28 eyes (60.7%) upon final follow-up. All papilledema resolved postoperatively. No complications were reported except for one transient postoperative diplopia. The median ADL score was 100 (range 25–100), and the mean total VFQ-25 score was 40.6 (range 9.5–87.3). Conclusion This was the largest study to describe ONSF’s role in CVST based on a long-term follow-up. Considering its efficacy and favorable safety, ONSF can be considered an important adjunctive approach to resolving progressive visual loss of CVST patients, on the basis of anticoagulation and ICP-lowering therapy.